Burn shock. The following factors play an important role in its pathogenesis.

Firstly, Burn shock is characterized by severe pain, since burned tissues become a source of powerful pain impulses. As a result, the erectile phase of burn shock is extremely short-lived (it is usually not seen, since it ends before the doctor arrives or the patient is admitted to the hospital). Therefore, the torpid phase in burn shock is extremely difficult.

Secondly, during burn shock, BCC decreases due not only to vascular disorders, but also as a result of intense plasmorrhagia through the burned surface. The patient loses a huge amount of fluid and The degree of blood thickening during burn shock is significantly higher than during shock of any other etiology. Therefore, in case of burn shock, the patient should not be given a transfusion. whole blood, and plasma or saline solution, in order to dilute the red blood cell mass (blood replacement fluids containing high molecular weight colloids are preferred, which create high oncotic pressure in the vascular bed, restoring bcc).

Thirdly, in this situation there is intoxication due to the absorption of tissue decay products from the extensive wound surface. Therefore, the complex of therapeutic measures for burn shock necessarily includes detoxification of the body, which consists of administering large quantities of fluid containing glucose, vitamins, as well as hemodialysis and hemosorption.

Fourthly, the burned surface represents an extensive wound gate of infection, which requires appropriate measures (carrying out antibacterial therapy, keeping patients in rooms with sterile air, etc.).

Electric shock. This type of shock occurs as a result of electric shock and belongs to the group of painful shocks, which determines the complex of therapeutic measures. However, with electric shock there are a number of features that require special attention and specific therapy.

1. If electric current passed through the whole body or through chest, then the development of ventricular fibrillation of the heart is possible. Therefore, in this case, when providing first aid to such a victim, you should use indoor massage heart, and if the necessary equipment is available, electrical defibrillation of the heart. At the same time, artificial respiration is performed.

2. When an electric current passes through the head, profound depression of the respiratory and vasomotor centers is possible, and therefore it is often necessary to carry out artificial respiration and cardiac massage for hours until the activity of these centers is restored.

3. At the site of injury, the electric current causes electrolysis of tissues - appear current signs, which leads to the development of local injuries that take a long time to heal and are difficult to treat.

Cardiogenic shock. With a massive myocardial infarction, the patient may fall into a state of cardiogenic shock, the mortality rate of which reaches 90%. In the pathogenesis of this serious condition The following three factors play an important role:

1. Intense pain syndrome, arising as a result of ischemia of large areas of the myocardium and the accumulation of under-oxidized products in it.

2. Myocardial edema, developing as a result of a sharp increase in vascular-tissue permeability in the heart muscle.

3. Vascular insufficiency (collapse), which is an expression of total hemodynamic disturbances in the body during massive myocardial infarction.

In connection with the above, therapy for cardiogenic shock should, along with the elimination of pain, include measures to quickly reduce membrane permeability ( intravenous administration glucocorticoids), the degree of myocardial edema (use of diuretics, lymph drainage, including surgical drainage of the thoracic lymphatic duct) and normalization of vascular tone.

Blood transfusion shock. It occurs when incompatible blood is transfused to a patient. The resulting antigen-antibody complex is an extreme irritant for vascular interoreceptors, as a result of which a powerful flow of afferent impulses occurs into the higher nerve centers. This was proven by the following experiments (S. M. Pavlenko, 1942). A section of the animal was cut off blood vessel, connected to the body only by nerve trunks. If this segment was first washed of blood, and then foreign blood was introduced into it, then disorders of the body’s functions did not occur. If it contained one’s own blood, then when foreign blood was introduced into it, a picture of blood transfusion shock developed: the same injection into a previously denervated segment of the vessel did not lead to shock.

At blood transfusion shock It has its own clinical features associated with the fact that it causes hemolysis of red blood cells. The products of hemolysis damage the kidneys especially severely, and the patient, even having safely recovered from the state of transfusion shock, may die in more late period process in cases of renal failure. Therefore, the complex of therapeutic measures for blood transfusion shock must include hemodialysis and hemosorption.

As for the other types of shock given in the classification scheme, *****shem29 then their development is not fundamentally different from the pathogenesis of painful shock, and some features of the course are the subject of study of relevant clinical disciplines.

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Federal State Autonomous Educational

institution of higher professional education

"Belgorod State National Research University"

(National Research University "BelSU")

Medical Institute

Department of Pathology

Abstract on the topic:

Clinical pathophysiology of shock

Completed by: 4th year student

Faculty of General Medicine and Pediatrics

Groups 03011207 Kashichkina A.A.

Checked by: assistant of the Department of Pathology O.V. Konova.

Belgorod 2015

Introduction

2. Traumatic shock

3. Pathogenesis

4. Changes in the body

5. Rationale for therapy

References

shock traumatic clinical therapy

Introduction

Intensive development of the problem of shock began during the formation of capitalist society. Train accidents, industrial injuries and especially wars encouraged researchers to study shock. It is not difficult to see that every war stimulated scientific research on the problem of shock. During the wars of the 20th century, the governments of the warring countries were forced to take special measures to combat shock. For example, in the British army during the war of 1914 - 1918, a special committee was created to combat shock.

As a matter of fact, military doctors made the greatest contribution to the development of shock teachings. The description of shock was given by Hippocrates in the 24th aphorism, which drew attention to the development of delirium or stupor during traumatic brain injury.

The term shock itself, which is currently used very widely, has entered the literature very firmly. The author of this term is not precisely established, but most researchers believe that this concept, as applied to the reaction to severe mechanical trauma, first appeared in the English translation of the book by Louis XV's army consultant Le Dran (1737), made by Latta (1795).

1. The concept of shock and its etiology

Shock is a complex typical pathological process that occurs when the body is exposed to extreme factors of the external and internal environment, which, along with primary damage, cause excessive and inadequate reactions of adaptive systems. Shock is characterized by a stadium-like progressive disorder of the body's vital functions as a result of increasing dysfunction of the nervous, endocrine, cardiovascular, respiratory and other vital systems.

An important distinguishing feature of shock is that it is caused by an extreme factor of great damaging force, usually leading to varying degrees of destruction of the structural elements of tissues and organs.

Main causes of shock:

1) Various types of injuries (For example, mechanical destruction, ruptures, triples, tissue crushing, extensive burns, electrical injuries)

2) Massive Blood Loss

3) Transfusion of incompatible blood

4) Allergens entering the sensitized body

5) Extensive ischemia or necrosis of organs.

Depending on the cause of shock, they usually distinguish traumatic shock, burn, hemorrhagic, blood transfusion, anaphylactic, cardiogenic, psychogenic and others. Despite some differences in the clinical picture, all of the listed types of shock have the same pathogenesis. Based on this, let us consider the mechanism of shock development using the example traumatic shock.

2. Traumatic shock

Traumatic shock is a typical pathological process that occurs as a result of damage to organs, irritation of receptors and nerves of injured tissue, blood loss and the entry of biologically active substances into the blood, i.e. factors that together cause excessive and inadequate reactions of adaptive systems, especially the sympathetic-adrenal system, persistent disturbances in the neuroendocrine regulation of homeostasis, especially hemodynamics, disturbances in the specific functions of damaged organs, disorders of microcirculation, oxygen regime of the body and metabolism.

For the development of traumatic shock, conditions are of great importance external environment. Traumatic shock is caused by: overheating, hypothermia, malnutrition, mental trauma.

Some unique risk factors include: heredity, type nervous activity, age, diseases preceding the injury ( hypertension, physical inactivity, nervous mental stress, blood loss), alcohol intoxication.

It is very important to take into account the dynamics of traumatic shock - its phase development. The idea of two phases in the development of traumatic shock: the first, occurring after the injury and manifested by activation of functions, erectile, and the second, expressed by inhibition of functions, torpid, was given by N.I. Pirogov, and justifiably N.N. Burdenko.

The erectile shock phase - the arousal phase - is the initial stage of the reaction to severe damage. Externally, it is manifested by motor restlessness, screaming, pallor of the integument and mucous membranes, increased arterial and venous pressure, tachycardia, and sometimes urination and defecation. In this phase, as a result of generalized excitation and stimulation of the endocrine apparatus, metabolic processes are activated, while their circulatory support is insufficient. In this phase, prerequisites arise for the development of inhibition in the nervous system, circulation disorders, and oxygen deficiency occurs. The erectile phase is short-lived and usually lasts minutes.

The torpid phase of shock is a phase of depression that develops after the erectile phase, manifested by physical inactivity, hyporeflexia, significant circulatory disorders, in particular arterial hypotension, tachycardia, disorders external respiration(tachypnea at the beginning, bradypnea or periodic breathing at the end), oliguria, hypothermia, etc. In the torpid phase of shock, metabolic disorders are aggravated due to disorders of neurohumoral regulation and circulatory support. These violations in various organs are not the same. The torpid phase is the most typical and prolonged phase of shock; its duration can range from several minutes to many hours. In addition to the erectile and torpid phases of shock in severe shock ending in death, it is advisable to distinguish the terminal phase of traumatic shock, thereby emphasizing its specificity and difference from the pre-mortem stages of other pathological processes, usually united by the general term “terminal conditions”.

The terminal phase is characterized by certain dynamics: it begins to be revealed by disorders of external respiration (Biot or Kussmaul breathing), instability and sharp decline blood pressure, slow heart rate. The terminal phase of shock is characterized by a relatively slow development, and therefore a greater depletion of adaptation mechanisms, more significant than, for example, with blood loss, intoxication, and more profound dysfunction of organs. The restoration of these functions during therapy occurs more slowly.

According to the severity of the clinical course, mild shock, moderate shock and severe shock are distinguished. Along with this, shock is divided into four degrees. This division is based on the level of systolic blood pressure. I degree of shock is observed when the maximum blood pressure is above 90 mm Hg. Art. - mild stupor, tachycardia up to 100 beats/min, urination is not impaired. Blood loss: 15-25% of the total blood volume. II degree - 90-70 mm Hg. Art., stupor, tachycardia up to 120 beats/min, oliguria. Blood loss: 25-30% of the total blood volume. III degree - 70-50 mm Hg. Art., stupor, tachycardia more than 130-140 beats/min, no urination. Blood loss: more than 30% of the total blood volume. IV degree - below 50 mm Hg. Art., coma, pulse in the periphery is not determined, appearance pathological breathing, multiple organ failure, areflexia. Blood loss: more than 30% of the total blood volume. Should be regarded as terminal state. The clinical picture of shock is influenced by the type nervous system, gender, age of the victim, concomitant pathology, infectious diseases, history of trauma accompanied by shock. Important role play by blood loss, dehydrating diseases and conditions that affect the bcc and lay the basis for hemodynamic disorders. A shock index can be obtained to obtain a certain idea of the degree of decrease in blood volume and the depth of hypovolemic disorders. It can be calculated using the following formula: shock index = pulse rate / systolic blood pressure. Normally, the shock index is 0.5. If the index increases to 1 (pulse and blood pressure are equal to 100), approximately the decrease in blood volume is equal to 30% of the expected value; when it increases to 1.5 (pulse is 120, blood pressure is 80), the blood volume is 50% of the expected value, and with shock index values 2.0 (pulse - 140, blood pressure - 70) volume of circulating blood in active blood circulation, is only 30% of what it should be, which, of course, cannot provide adequate perfusion of the body and leads to high risk death of the victim. The main pathogenetic factors of traumatic shock can be identified as follows: inadequate impulses from damaged tissues; local blood and plasma loss; the entry into the blood of biologically active substances resulting from cell destruction and oxygen starvation of tissues; loss or dysfunction of damaged organs. Moreover, the first three factors are nonspecific, that is, inherent in any injury, and the last characterizes the specificity of the injury and the shock that develops.

3. Pathogenesis

The traumatic factor acts on organs and tissues, causing their damage. As a result, cell destruction occurs and their contents escape into the intercellular environment; other cells are subject to contusion, as a result of which their metabolism and inherent functions are disrupted. Primary (due to the action of a traumatic factor) and secondary (due to changes in the tissue environment) numerous receptors in the wound are irritated, which is subjectively perceived as pain, but objectively characterized by numerous reactions of organs and systems. Inadequate impulses from damaged tissues have a number of consequences. 1. As a result of inadequate impulses from damaged tissues, a pain dominant is formed in the nervous system, which suppresses other functions of the nervous system. Along with this, a typical defensive reaction occurs with stereotypical autonomic accompaniment, since pain is a signal to flee or fight. The basis of this autonomic reaction essential components are: release of catecholamines, increased pressure and tachycardia, increased breathing, activation of the hypothalamic-pituitary-adrenal system. 2. The effects of painful stimulation depend on its intensity. Weak and moderate irritation causes stimulation of many adaptive mechanisms (leukocytosis, phagocytosis, increased function of the SFM, etc.); severe irritation inhibit adaptive mechanisms. 3. Reflex tissue ischemia plays an important role in the development of shock. In this case, under-oxidized products accumulate, and the pH decreases to values borderline acceptable for life. On this basis, microcirculation disorders, pathological blood deposition, and arterial hypotension occur. 4. Pain and the entire situation at the time of injury certainly cause emotional stress, mental tension, and a feeling of anxiety about danger, which further enhances the neurovegetative reaction.

4. Changes in the body

The role of the nervous system.

When the body is exposed to a damaging mechanical agent in the damaged area, various nerve elements are irritated, not only receptors, but also other elements - nerve fibers passing through the tissues that make up the nerve trunks. While the receptors have a known specificity in relation to the stimulus, characterized by differences in the threshold value for different stimuli, the nerve fibers in relation to mechanical stimulation do not differ so sharply from each other, therefore mechanical stimulation causes excitation in the conductors various kinds sensitivity, and not just pain or tactile. This is precisely why injuries accompanied by crushing or rupture of large nerve trunks are characterized by more severe traumatic shock. The erectile phase of shock is characterized by generalization of excitation, which is externally manifested in motor restlessness, speech excitation, screaming, and increased sensitivity to various stimuli. Excitation also covers the autonomic nerve centers, which is manifested by an increase in the functional activity of the endocrine apparatus and the release of catecholamines, adaptive and other hormones into the blood, stimulation of heart activity and an increase in the tone of resistance vessels, activation of metabolic processes. Prolonged and intense impulses from the site of injury, and then from organs with impaired functions, changes in the lability of nerve elements due to disorders of blood circulation and oxygen regime determine the subsequent development of the inhibitory process. The irradiation of excitation - its generalization - is a necessary prerequisite for the occurrence of inhibition. Of particular importance is the fact that inhibition in the zone of the reticular formation protects the cerebral cortex from the flow of impulses from the periphery, which ensures the safety of its functions. At the same time, elements of the reticular formation that facilitate the conduction of impulses (RF+) are more sensitive to circulatory disorders than those that inhibit the conduction of impulses (RF-). It follows from this that circulatory disorders in this area should contribute to a functional blockade of impulse conduction. Gradual inhibition extends to other levels of the nervous system. It tends to deepen due to impulses from the area of injury.

Role endocrine system.

Traumatic shock is also accompanied by changes in the endocrine system (in particular, the hypothalamic-pituitary-adrenal system). During the erectile phase of shock, the content of corticosteroids in the blood increases, and during the torpid phase, their amount is reduced. However, the adrenal cortex remains responsive to externally administered ACTH. Consequently, the inhibition of the cortical layer is largely due to the insufficiency of the pituitary gland. Hyperadrenalineemia is very typical for traumatic shock. Hyperadrenalineemia, on the one hand, is a consequence of intense afferent impulses caused by damage, on the other hand, a reaction to gradual development arterial hypotension.

Local blood and plasma loss.

For any mechanical injury there is a loss of blood and plasma, the extent of which is very variable and depends on the degree of tissue trauma, as well as on the nature of vascular damage. Even with a minor injury, exudation into the injured tissue is observed due to the development inflammatory reaction, and hence loss of fluid. However, the specificity of traumatic shock is still determined by neuropainful injury. Neuropainful injury and blood loss are synergistic in their effect on the cardiovascular system. With painful stimulation and loss of blood, vasospasm and the release of catecholamines first occur. With blood loss immediately, and with painful stimulation later, the volume of circulating blood decreases: in the first case due to exit from the vascular bed, and in the second - as a result of pathological deposition. It should be noted that even small bloodletting (1% of body weight) sensitizes (increases the body’s sensitivity) to mechanical damage.

Circulatory disorders.

The very concept of “shock” includes mandatory and severe violations hemodynamics. Hemodynamic disturbances during shock are characterized by sharp deviations in many parameters of the systemic circulation. Disorders of systemic hemodynamics are characterized by three cardinal signs - hypovolemia, decreased cardiac output and arterial hypotension. Hypovolemia has always been considered important in the pathogenesis of traumatic shock. On the one hand, it is caused by blood loss, and on the other, by the retention of blood in capacitive vessels (venules, small veins), capillaries - by its deposition. The exclusion of some blood from circulation can be clearly detected already at the end of the erectile shock phase. By the beginning of the development of the torpid phase, hypovolemia is even more pronounced than in subsequent periods. One of the most typical symptoms traumatic shock are phase changes in blood pressure - its increase in the erectile phase of traumatic shock (the tone of resistive and capacitive vessels increases, as evidenced by arterial and venous hypertension), as well as a short-term increase in the volume of circulating blood, combined with a decrease in the capacity of the functioning vascular bed of the organs. The increase in blood pressure, typical for the erectile phase of traumatic shock, is the result of an increase in total peripheral vascular resistance due to activation of the sympathoadrenal system. An increase in the tone of resistive vessels is combined with the activation of arteriovenous anastomoses and the ejection of blood from the high-pressure vascular system (arterial bed) into the vascular system low pressure (venous bed), which leads to an increase in venous pressure and prevents the outflow of blood from the capillaries. If we take into account the fact that most capillaries do not have sphincters at their venous end, then it is not difficult to imagine that under such conditions not only direct, but also retrograde filling of the capillaries is possible. Numerous researchers have shown that hypovolemia limits afferent impulses from baroreceptors (stretch receptors) of the aortic arch and sinocarotid zone, as a result of which the pressor formations of the vasomotor center are excited (disinhibited) and spasm of arterioles occurs in many organs and tissues. Sympathetic efferent impulses to the blood vessels and heart are enhanced. As blood pressure decreases, tissue blood flow decreases, hypoxia increases, which causes impulses from tissue chemoreceptors and further activates the sympathetic effect on the vessels. The heart empties more completely (residual volume decreases), and tachycardia also occurs. A reflex also arises from the vascular baroreceptors, leading to an increased release of adrenaline and norepinephrine by the adrenal medulla, the concentration of which in the blood increases 10-15 times. In a later period, when renal hypoxia develops, vascular spasm is maintained not only by increased secretion of catecholamines and vasopressin, but also by the release of renin by the kidneys, which is the initiator of the renin-angiotensin system. It is believed that this generalized vasoconstriction does not involve the vessels of the brain, heart and liver. Therefore, this reaction is called centralization of blood circulation. Peripheral organs are increasingly suffering from hypoxia, as a result of which metabolism is disrupted and under-oxidized products and biologically active metabolites appear in the tissues. Their entry into the blood leads to acidosis of the blood, as well as the appearance of factors in it that specifically inhibit the contractility of the heart muscle. Another mechanism is also possible here. The development of tachycardia leads to a reduction in diastole time - the period during which coronary blood flow occurs. All this leads to disruption of myocardial metabolism. With the development of the irreversible stage of shock, the heart can also be affected by endotoxins, lysosomal enzymes and other biologically active substances specific to this period. Thus, blood and plasma loss, pathological blood deposition, and fluid extravasation lead to a decrease in the volume of circulating blood and a decrease in venous blood return. This, in turn, along with metabolic disorders in the myocardium and a decrease in the performance of the heart muscle leads to hypotension, characteristic of the torpid phase of traumatic shock. Vasoactive metabolites that accumulate during tissue hypoxia disrupt the function of vascular smooth muscles, which leads to a decrease in vascular tone, and therefore to a drop in the overall resistance of the vascular bed and, again, to hypotension.

Disorders of capillary blood flow deepen as a result of a violation of the rheological properties of blood, aggregation of red blood cells, which occurs as a result of increased activity of the coagulation system and thickening of the blood due to the release of fluid into the tissue. Breathing disorders. In the erectile stage of traumatic shock, frequent and deep breathing. The main stimulating factor is irritation of the receptors of injured tissues, which causes excitation of the cerebral cortex and subcortical centers, is excited and respiratory center medulla oblongata.

Abnormalities in the lungs and the effects they cause are combined into a symptom complex called respiratory distress syndrome. This acute disorder pulmonary gas exchange with life-threatening severe hypoxemia as a result of a decrease to a critical level and below the number of normal respirons (respiron is a terminal or final respiratory unit), which is caused by negative neurohumoral influences (neurogenic spasm of pulmonary microvessels during pathological pain), damage to the pulmonary capillary endothelium with cytolysis and destruction of intercellular connections, migration shaped elements blood (primarily leukocytes), plasma proteins into the pulmonary membrane, and then into the lumen of the alveoli, the development of hypercoagulation and thrombosis of the pulmonary vessels.

Metabolic disorders. Energy exchange.

Shock of various etiologies through microcirculation disorders and destruction of the histohematic barrier (exchange capillary - interstitium - cell cytosol) critically reduces oxygen delivery to mitochondria. As a result, rapidly progressing disorders of aerobic metabolism occur. The links in the pathogenesis of dysfunctions at the level of mitochondria in shock are: swelling of mitochondria, disorders enzyme systems mitochondria due to a deficiency of necessary cofactors, a decrease in magnesium content in mitochondria, an increase in calcium content in mitochondria, pathological changes in the content of sodium and potassium in mitochondria, disorders of mitochondrial functions due to the action of endogenous toxins (free fatty acids, etc.), free radical oxidation of phospholipids in mitochondrial membranes. Thus, during shock, the accumulation of energy in the form of high-energy phosphorus compounds is limited. Accumulates large number inorganic phosphorus that enters the plasma. Lack of energy disrupts the function of the sodium-potassium pump, causing excess sodium and water to enter the cell and potassium to leave the cell. Sodium and water cause mitochondria to swell, further uncoupling respiration and phosphorylation. As a result of decreased energy production in the Krebs cycle, the activation of amino acids is limited, and as a result, protein synthesis is inhibited. A decrease in ATP concentration slows down the combination of amino acids with ribonucleic acids (RNA), the function of ribosomes is disrupted, resulting in the production of abnormal, incomplete peptides, some of which may be biologically active. Severe acidosis in the cell causes rupture of lysosome membranes, as a result of which hydrolytic enzymes enter the protoplasm, causing the digestion of proteins, carbohydrates, and fats. The cell dies. As a result of insufficient cell energy and metabolic disorders, amino acids enter the blood plasma, fatty acids, phosphates, lactic acid. Apparently, mitochondrial dysfunctions (like any pathological processes) develop in different organs and tissues asynchronously, mosaically. Damage to mitochondria and disorders of their functions are especially pronounced in hepatocytes, while in neurons of the brain they remain minimal even in decompensated shock.

It should be noted that mitochondrial damage and dysfunction are reversible in compensated and decompensated shock and are reversed by rational analgesia, infusions, oxygen therapy and hemorrhage control.

Carbohydrate metabolism. During the erectile phase of traumatic shock, the concentration of insulin antagonists, catecholamines, which stimulate the breakdown of glycogen, glucocorticoids, which enhance the processes of gluconeogenesis, thyroxine and glucagon, increases in the blood as a result of increased activity endocrine glands. In addition, the excitability of the sympathetic nervous system (hypothalamic centers) is increased, which also contributes to the development of hyperglycemia. In many tissues, glucose consumption is inhibited. In general, a false-diabetic picture is revealed. IN late stages shock, hypoglycemia develops. Its origin is connected with full use liver glycogen reserves available for consumption, as well as a decrease in the intensity of gluconeogenesis due to the use of substrates necessary for this and relative (peripheral) corticosteroid deficiency.

Lipid metabolism. With changes carbohydrate metabolism Disorders of lipid metabolism, manifested in the torpid phase of shock by ketonemia and ketonuria, are closely associated. This is explained by the fact that fats (as one of the main energy sources) are mobilized from the depot during shock (their concentration in the blood increases), and oxidation is not complete.

Globulins, which, as is known, are directly related to the vasoactive properties of blood. The accumulation of nitrogenous products and changes in the ionic composition of plasma contribute to impaired renal function. Oliguria, and in severe cases of shock, anuria are constant during this process. Renal dysfunction usually corresponds to the severity of shock. It is known that with a decrease in blood pressure to 70-50 mm Hg. Art. the kidneys completely stop filtering in the glomerular apparatus of the kidney due to changes in the relationships between hydrostatic, colloidosmotic and capsular pressure. However, in traumatic shock, renal dysfunction is not solely a consequence arterial hypotension: Shock is characterized by restriction of cortical circulation due to increased vascular resistance and shunting through the juxtaglomerular pathways. This is determined not only by a decrease in cardiac performance, but also by an increase in the tone of the vessels of the cortical layer.

Protein metabolism. A manifestation of its disturbance is an increase in the content of non-protein nitrogen in the blood, mainly due to polypeptide nitrogen and, to a lesser extent, urea nitrogen, the synthesis of which is disrupted with the development of shock. Changes in the composition of serum proteins during traumatic shock are expressed by a decrease in their total number mainly due to albumin. The latter may be associated both with metabolic disturbances and with changes in vascular permeability. It should be noted that with the development of shock, the content of ion exchange in the serum increases. Significant shifts are detected in the ionic composition of the plasma. With traumatic shock, a gradual convergence occurs, the concentration of ions in the cells and extracellular fluid, while normally the ions K+, Mg2+, Ca2+, HPO42-, PO43- predominate in the cells, and in the extracellular fluid Na+, C1-, HCO3-. Receipt of biologically active substances into the blood. For the subsequent course of the process, the release of active amines from cells, which are chemical mediators of inflammation, is of great importance. Currently, over 25 such mediators have been described. The most important of them, appearing immediately after damage, are histamine and serotonin. With extensive tissue damage, histamine can enter the general bloodstream, and since histamine causes dilation of precapillaries and spasm of veins without directly affecting the capillary bed, this leads to a decrease in peripheral vascular resistance and a drop in blood pressure. Under the influence of histamine, channels and gaps are formed in the endothelium, through which blood components, including cellular elements (leukocytes and erythrocytes), penetrate into the tissues. As a result of this, exudation and intercellular edema occur. Under the influence of injury, the permeability of vascular and tissue membranes increases, but still due to circulatory disorders, absorption from injured tissues various substances slows down. Enzymes of lysosomes of tissue cells and neutrophils play a major role in the development of secondary alteration. These enzymes (hydrolases) have pronounced proteolytic activity. Along with these factors, plasma kinins (bradykinin), as well as prostaglandins, play a certain role in circulatory disorders. These factors also affect the microcirculation system, causing expansion of arterioles, capillaries and an increase in their permeability, which occurs first (mainly in venules) due to the formation of intercellular gaps and transendothelial channels. Later, the permeability of the capillary and precapillary sections of the vascular bed changes.

5. Principles of therapy

The basic principle of treating shock is the complexity of therapy. Taking into account the phases of shock development is important in the treatment of shock. The treatment carried out should be as fast and vigorous as possible. When treating shock in the erectile phase, when circulatory disorders have not yet fully developed, deep hypoxia and advanced metabolic disorders have not yet occurred, measures should be limited to preventing their development. During this phase, means that limit afferent impulses are widely used; various types of novocaine blockades, analgesics, neuroplegics, narcotic substances. Analgesics that inhibit impulse transmission, suppress autonomic reactions, and limit the feeling of pain are indicated in early periods of shock. An important point, limiting impulses from the site of damage is rest of the damaged area (immobilization, bandages, etc.). During the erectile shock phase, it is recommended to use saline solutions containing neurotropic and energetic substances (liquids of Popov, Petrov, Filatov, etc.). Significant disorders of circulation, tissue respiration and metabolism that occur in the torpid phase of shock require various measures aimed at their correction. To correct circulatory disorders, blood transfusions or blood substitutes are used. In severe shock, intra-arterial transfusions are more effective. Their high efficiency associated with stimulation of vascular receptors, increased capillary blood flow and the release of part of the deposited blood. Due to the fact that during shock there is predominantly deposition of formed elements and their aggregation, it seems very promising to use low molecular weight colloidal plasma substitutes (dextrans, polyvinol), which have a disaggregating effect and reduce blood viscosity at low shear stresses. Caution should be exercised when using vasopressor agents.

Hormones - ACTH and cortisone, administered to normalize metabolic processes, have a noticeable effect on blood flow during traumatic shock. During the development of shock, relative and then absolute adrenal insufficiency is detected first. In light of these data, the use of ACTH appears to be more appropriate in the early stages of shock or in its prevention. Glucocorticoids administered in the torpid phase have a diverse effect. They change the response of blood vessels to vasoactive substances, in particular they potentiate the effect of vasopressors. In addition, they reduce vascular permeability. And yet, their main effect is associated with the influence on metabolic processes and, above all, on the metabolism of carbohydrates. Restoration of oxygen balance in conditions of shock is ensured not only by restoration of circulation, but also by the use of oxygen therapy. IN lately Oxygen barotherapy is also recommended. In order to improve metabolic processes, vitamins are used (ascorbic acid, thiamine, riboflavin, pyridoxine, calcium pangamate). Due to the increased resorption of biogenic amines and, above all, histamine from damaged tissues, the use of antihistamines. An essential place in the treatment of shock is occupied by the correction of acid-base balance. Acidosis is typical of traumatic shock. Its development is defined as metabolic disorders, and the accumulation of carbon dioxide. The development of acidosis is also facilitated by disruption of excretory processes. To reduce acidosis, the use of sodium bicarbonate is recommended; some consider the use of sodium lactate or Tris buffer to be better.

List of used literature

1. Litvitsky P.F. Pathophysiology: textbook in 2 volumes; Moscow, "GEOTAR-MED", 2003.

2. Chereshnev V.A., Yushkov B.G. Pathophysiology: textbook; Moscow, “VECHE”, 2001.

3. Ado A.D., Novitsky V.V. Pathological physiology, textbook; Tomsk, "TSU" 1997.

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Shock

Shock(from English schosk - blow, shock) is an acute general reflex reaction of the body in response to an extreme stimulus, characterized by a sharp depression of all vital functions due to disorders of their neurohumoral regulation. This is one of the common forms of pathology of the body. Suffice it to say that a significant proportion of patients admitted by ambulance are in a state of more or less severe shock, and from 10 to 30% of such patients cannot be saved. The amount of shock is especially large during the period of hostilities. Treatment of severe forms of shock is an extremely difficult task. All this determines the high relevance of this problem.

Shock can occur under the influence of stimuli of a very different nature, but characterized by extraordinary, excessive force - extreme. The cause of shock can be: severe mechanical trauma, extensive burns of the second and third degrees, entry into the body of heterogeneous or incompatible blood for certain factors, repeated parenteral administration of foreign protein and other substances of an antigenic nature, powerful effects of ionizing radiation, electrical trauma, severe mental trauma, etc. .p.

All kinds of adverse effects on the body that precede the shock stimulus, act together with it or after it facilitate the occurrence of shock and aggravate the already developed shock. Such additional factors include blood loss, overheating or hypothermia of the body, prolonged physical inactivity, fasting, overwork, nervous overstrain, mental trauma, and even such seemingly indifferent stimuli as bright light, loud conversation, etc. For example, during the Great Patriotic War, it was found that shock when wounded more often developed and was more severe in soldiers who were assigned the most dangerous tasks: clearing roads, reconnaissance, etc. Other things being equal, shock more often occurs in children under 14 years of age and in people over 60 years of age compared to middle-aged people.

The course of shock is more favorable in children and especially unfavorable in the elderly. Unfavorable meteorological conditions also contribute to the development of shock: sudden changes in pressure, temperature, magnetic storms.

This pattern is widely used by experimenters when modeling shock, especially traumatic and burn shock, the modeling methods of which, unfortunately, are extremely cruel. The experiment is carried out without anesthesia (anesthesia significantly distorts the clinical picture, and, therefore, the mechanisms of development of the process; in some cases it is not possible to obtain shock at all under anesthesia), it requires an extremely strong painful, usually long-term effect. To limit the suffering of experimental animals, 3 days before the experiment they are transferred to a starvation diet, and immediately before the injury a small bloodletting is done. This allows you to get a severe form of shock, significantly reducing the time of pathogenic exposure.

Depending on the cause of shock, the following types are distinguished: traumatic, operating or surgical, burn, anaphylactic, blood transfusion, cardiogenic, electrical, radiation, psychogenic or mental, etc. Crash syndrome or crush syndrome is close to shock.

Until recently, the problem of shock was not considered in its entirety. Different types of shock were considered in different departments, in different departments of the same course. Thus, traumatic shock was discussed by surgeons and pathophysiologists in the section “mechanical injury”, and burn shock, which is so close to it, was discussed in the section “burns” or “thermal factors”, anaphylactic shock – in the section “Anaphylaxis”, etc. Thus, it was emphasized that different types of shock are different not only in the reasons that cause them, in the methods of reproduction in the experiment, but differ fundamentally, essentially, in terms of the basic patterns of their development. This is not true. The purpose of this chapter is not only to consider such a common form of severe pathology as shock, to highlight the features of the clinical picture and pathogenesis of various types of shock, but also to show that all types of shock ultimately develop according to the same general patterns.

Let us first turn to traumatic shock, as it is the most common shock in both peace and war.

Traumatic shock occurs when a large mass of soft tissue is crushed, skeletal bone fractures, damage to the chest or abdominal cavity, gunshot wounds, etc.

There are two stages in the development of shock: erectile and torpid. Distinctive Features erectile stages are: general excitement, motor reaction, speech anxiety, increased arterial blood pressure, shortness of breath, activation of metabolic processes, there may be an increase in body temperature, leukocytosis, etc. This stage of shock is very short-lived and usually does not exceed 10-15, less often 30 minutes. For the second, torpid stages are characteristic: pallor of the skin, cold sweat, sharp depression of the psyche, apathy, indifference to the environment with preserved consciousness, a progressive drop in blood pressure and an increasing weakening of cardiac activity, superficial, uneven in rhythm and depth, often periodic (Cheyne-Stokes, Biotta type) breathing, mixed type hypoxia, hypothermia, leukopenia with a shift of the leukocyte formula to the left, oliguria or anuria. The intensity of metabolic processes decreases. The body switches to an uneconomical, wasteful way of obtaining energy - glycolysis, as a result of which under-oxidized metabolic products accumulate (lactic, pyruvic acids), increasing acidosis develops, which initiates the formation of microthrombi in the vascular bed, sometimes resulting in the development of disseminated intravascular coagulation syndrome. In case of an unfavorable outcome, the third develops - terminal stage with all the periods and features inherent in the terminal state.

So, one of the features of shock is the staged nature of its development, which in traumatic shock is usually quite well expressed.

For the first time, a classical description of the picture of traumatic shock, both of its stages, was given by N.I. Pirogov. This is how he describes the initial manifestations of shock: “If a strong scream and groan is heard from a wounded person whose features have changed, his face has become long and convulsively twisted, pale or blue and swollen from screaming, if his pulse is tense, fast, his breathing is short and frequent , then no matter what its damage, you need to rush with help. Sometimes in these cases, when examining the wound, an open fracture of the bone is discovered, pressing on the nerve; the wound can be a bullet, and, apparently, the most ordinary one, but was broken due to careless transport. the bone is out of position and, irritating the nerve, causes unbearable torment; the pain may depend on the bent bullet, which is lodged directly on the nerve.”

The picture of the torpid station is described even more vividly: “With a torn off leg or arm, a man lies numb at the dressing station, motionless; he does not scream, does not scream, does not complain, does not take part in anything and does not demand anything; the body is cold, the face is pale, like the corpse; the gaze is motionless and directed into the distance, the pulse, like a thread, is barely noticeable under the finger and with frequent alternations. The numb man either does not answer questions at all, or only in a barely audible whisper, the breathing is also barely noticeable; the wound and skin are almost completely insensitive; but if the diseased nerve hanging from the wound is irritated by something, then the patient with one slight contraction of the personal muscles detects a sign of feeling. Sometimes this condition disappears after a few hours from the use of stimulants, but sometimes it continues until death. consciousness; it’s not that he is not at all aware of his suffering; he seems to be completely immersed in it, as if he has become silent and numb in it.” " Traumatic rigor mortis", "traumatic stupor", "traumatic numbness" - these are the terms used by N.I. Pirogov to characterize this stage of shock and which reflect the pathogenetic essence of the process in the best possible way.

Pathogenesis traumatic shock is complex. Many aspects of it still remain controversial. To date, about 20 theories of shock are known. Most of them have already lost scientific interest and have only historical significance. However, we need to dwell on two in order to understand the modern interpretation of the pathogenesis of shock.

The oldest and most stable theory is toxemia (V. Cannon), according to which shock occurs as a result of the action on the body of toxins released from destroyed tissues and formed as a result of metabolic disorders. Today it has been proven that intoxication occurs in the injured body. It is associated not only and not even so much with the death of injured tissues (as V. Cannon believed) and the formation in connection with this of large quantities of histamine and other biologically active substances, but also with a violation of the permeability of lysosomal membranes of ischemic tissues and the release of hydrolases into the general bloodstream, increased absorption of phenol, skatole, ammonia compounds, endotoxin of intestinal bacteria, impaired excretory function of the kidneys and the neutralizing function of the liver. The main cause of toxemia is considered to be the inability to remove toxic metabolic products due to tissue hypoperfusion and impaired renal function. A significant restriction of organ renal blood flow, observed already in the erectile stage of shock, increases sharply in the torpid stage. Volumetric blood flow through the kidneys decreases by 7 times or more, a redistribution of blood flow occurs (discharge of arterial blood through the arcuate arteries of the pyramids), which leads to catastrophic bleeding of the cortical layer, almost complete cessation of the filtration process, oliguria, and in more severe cases, anuria, dystrophic, and then necrotic changes, culminating in the development of acute renal failure (" shock bud "). However, 1) the development of toxemia takes time, and shock often occurs immediately after injury; 2) absorption from damaged tissues is slowed down (introducing a double lethal dose of strychnine into the injured limb does not cause the death of the animal); 3) does not confirm initiating the role of toxemia in the development of shock and experiments with cross-circulation. Recognizing the significant contribution of the latter to the mechanism of shock formation, it should be considered that it is not the initial link in its pathogenesis.

According to the second, fairly widespread theory of shock - theories of blood and plasma loss (Bla1osk), the leading link in its development is blood and plasma loss, which always occurs to one degree or another during massive trauma, if not due to visible blood loss, then as a result of tissue edema and hemorrhages into the injured tissue, i.e. hypovolemia, discrepancy between the volume of circulating blood and the volume of the vascular bed. Otherwise, shock was identified with the state after massive blood loss. Disputes over the validity of this identification continued for a long time. Until now, some authors (mostly foreign) call the condition that occurs after acute massive blood loss hemorrhagic shock, other hemorrhagic collapse. The fact is that the late picture of shock and the consequences of heavy blood loss are very similar. It has been established, however, that if the same hypotension (the most important criterion for the severity of shock and collapse) is achieved under experimental conditions on animals by inflicting extensive trauma not accompanied by bleeding and by massive bloodletting, it is much easier, with the help of blood transfusion, to remove an organism from a dangerous state that has lost a lot blood than an injured body without blood loss. In the second case, blood transfusion gives only a temporary positive effect. It must be assumed that the pathogenesis of these two conditions is unequal.

Today it has the greatest recognition neurogenic shock theory , the founder of which is N.I. Pirogov, then supported by a number of foreign scientists, developed in detail in subsequent works by I.R. Petrov, V.K. Kulagin, N.N. Gordienko, S.A. Seleznev and others. Its essence boils down to the following.

The initial link in the development of shock is the flow into the central nervous system of a huge number of impulses (primarily pain), caused by irritation of a mass of nerve receptors by an extremely strong stimulus and direct damage to the nerve trunks and the development as a result of this generalized excitation of the cortex and subcortical centers of the brain with all the ensuing consequences: activation of activity endocrine glands, increased release of hormones, including catecholamines, pituitary and thyroid hormones, increased blood pressure, shortness of breath, intensified metabolism, etc. The clinical expression of excitation in the central nervous system is erectile shock stage. Overexcitation of nerve cells is replaced by their inhibition and transition to its second stage - torpid. Initially, inhibition occurs in the reticular formation of the brain. The associated blockade of afferent impulses to the cerebral cortex can be regarded as a compensatory reaction of the body, temporarily protecting the central structures of the nervous system from asthenia. At the same time, blocking the channel of ascending impulses leads to disruption of the integrative activity of the brain, thus creating the preconditions for the cessation of the existence of the organism as a whole.

Of essential importance in the pathogenesis of shock at all stages of its development is the discrepancy between the needs of metabolism and its circulatory support caused by the disorder of regulation.. Excitation of the vasomotor center, excessive release of catecholamines, thyroid hormones at the first stage of shock lead to generalized vasoconstriction (with the exception of the vessels of the brain, heart, and partly the liver), blood pressure rises, arteriovenous anastomoses open, and a significant part of the blood enters the veins through arteriovenous shunts, bypassing capillary bed. This phenomenon is called blood flow shunting , is a clear reflection of the dual nature of the pathological process. On the one hand, it leads to an increase in the number of blood recirculations, which, against the background of the absence of spasm of the blood vessels of the brain and heart, provides a relatively favorable blood supply to these vital organs (“ centralization of blood circulation ") and is thus compensatory in nature. On the other hand, the transition of blood from arteries with a high level of pressure to the veins significantly increases the pressure in them, as a result of which the outflow of blood into the veins from the capillaries is hampered. The developing peculiar hydraulic seal leads to capillary blood flow slows down, and the supply of oxygen to tissues is increasingly disrupted. Increasing tissue hypoxia is aggravated by increased metabolic processes (due to stimulation of the central nervous system, the hypothalamus, in particular). The difficulty of blood outflow into the veins is also associated with pathological deposition. a significant part of the blood in the capillary bed and a decrease in the mass of circulating blood. Already by the end of the erectile stage of shock, up to 20-30% of the blood is excluded from the general circulation. Taking into account that the injury is usually accompanied by more or less significant blood loss, it becomes obvious that the return. blood to the heart, and at the same time the stroke volume of blood drops sharply. Due to moderate tachycardia, the minute blood volume is maintained for some time at a relatively tolerable level. Significant tachycardia (up to I60-I80 beats per minute at the stage of advanced shock), on the contrary, aggravates the situation, since the diastole period is sharply reduced, and the cavities of the heart do not have time to fill with blood. The heart, wasting energy on contractions, runs idle. The minute volume of blood not only does not increase, but falls even more sharply. Initially, a compensatory-adaptive reaction (increased heart contractions) when it is excessively expressed turns into its opposite and becomes a pathological reaction.

When shock passes into the torpid stage, high vascular tone is replaced by hypotension, numerous vicious circles are formed, as a result of which the imbalance of hemodynamics and metabolism reaches such a degree that the reverse development of the process often becomes impossible.

An undoubted contribution to the development of shock is made by increasing toxemia (see page), blood and plasma loss, which, as a rule, accompany injury to a greater or lesser extent.

A very dangerous, often life-threatening disorder of the patient, is a violation of the gas exchange function of the lungs (" shock lung "). The shunting of blood flow, characteristic of shock, accompanied by a sharp disorder of microcirculation, leads to swelling of the alveolo-capillary membranes, the development of interstitial edema, a sharp deterioration in the diffusion process, catastrophically aggravating the consequences of ventilation-perfusion disorders associated with changes in the rhythm, depth and frequency of breathing.

The second most common form of shock is burn. The frequency of its development is closely related to the area of tissue affected by the burn and the degree of burn injury. It is believed that with second and third degree burns occupying less than 10% of the body, the development of shock is unlikely; in the future, the probability of developing shock is equal to the area of the burn multiplied by 2; with an area equal to 20% of the body, shock develops in approximately 40% of cases, a lesion of 30% is accompanied by shock in 60% of cases, etc. Other distinctive features of burn shock are often a long duration (up to 1-2 hours) of the erectile stage, a greater share in the mechanism of its development of toxemia (due to tissue death, violations of the barrier properties of the skin, infection), as well as blood and plasma loss due to damage to a significant number of blood and lymphatic vessels. The latter leads to an imbalance in water balance, extracellular dehydration, thickening of the blood, and an increase in its viscosity, which makes blood microperfusion even more difficult with all the ensuing consequences. The leading factor in the pathogenesis of this form of shock, however, is the flow of pain impulses into the central nervous system., with which impulses from vascular chemo- and baroreceptors are summed up in connection with toxemia and increasing oligemia. In later stages of burn disease, auto-allergic processes associated with the formation of a large number of altered proteins may occur.

Cardiogenic shock occurs as a severe complication of angina and myocardial infarction in the acute period of its development and is the main cause of death in these conditions. Before the advent of vasopressors and other means of treating it, 80% of patients with cardiogenic shock died. Hypoxia of the heart muscle during spasm of the coronary vessels is accompanied by a severe pain attack. The flow of pain impulses in combination with emotionally caused (feelings of fear during pain in the heart) dysfunction of the central nervous system underlies its development. Due to the weakening of the contractile function of the myocardium caused by trophic disorders, the IOC is significantly reduced. The erectile stage in this form of shock, although usually not very pronounced, is characterized by a special duration, often lasting for hours. Then the patient’s condition and heart function suddenly deteriorate, nausea and vomiting appear, signaling the transition of shock to stage II. Blood pressure drops, increasing tachycardia is noted, and various types of arrhythmias often occur. In the lungs, in addition to the usual changes for shock, in case of severe left ventricular failure, edema develops.

Anaphylactic shock develops in response to repeated parenteral administration of a foreign protein or to the entry into the body of other substances of an antigenic nature. Factors that provoke the development of this form of shock may include medications (antibiotics, analgesics, sulfa drugs, novocaine, etc.), with an increase in the number of which the number of cases of anaphylactic shock also increases. The factor initiating the development of this form of shock is the formation of antigen-antibody complexes. Shock occurs suddenly, within a few minutes. The erectile stage is usually very short-lived and elusive. It manifests itself as a feeling of anxiety, motor agitation, and headache. Then a spasm of smooth muscles (especially the muscles of the bronchi) occurs, convulsions and asphyxia appear. It is difficult and without timely intensive care quickly ends in death.

Blood transfusion shock occurs after transfusions of incompatible blood. According to the mechanism of development and clinical picture, it is close to anaphylactic: very short-term, sometimes elusive, erectile stage, early catastrophic drop in blood pressure, bronchospasm and difficulty breathing, severe impairment of kidney function, rapid onset of death. Harbingers of shock are dizziness, headache, sharp, unbearable pain in the lumbar region and calf muscles that occur after a blood transfusion, and sometimes already during the transfusion, caused by selective vasospasm. The triggers in the development of this form of shock are massive agglucination of blood cells, red blood cells, in particular, their subsequent hemolysis, colloid-clasic changes (mutual precipitation of blood proteins of the donor and recipient).

The protective effect on the development of these two forms of shock (anaphylactic and blood transfusion) of deep anesthesia, the possibility of obtaining them in an experiment by irrigation with heterogeneous blood or anaphylactogenic substances of the vessels of isolated organs (spleen, limb, carotid sinus), which have retained communication with the body only through nerves, and prevention This effect by preliminary novocainization of the vessels of these organs indicates in favor of a decisive role in their development of neuroreflex mechanisms.

Psychogenic shock is provoked by severe mental trauma, negative emotions, and occurs more easily in people with a weak type of higher nervous activity, altered reactivity. In people with increased sensitivity to pain and a special type of nervous system, who have experienced severe pain during surgery, tooth extraction, its treatment, etc., shock can develop conditionally reflexively at the sight of surgical instruments, a drill, the operating room environment, etc. Mental stress facilitates the development of other forms of shock: traumatic, surgical, cardiogenic, burn, etc.

Summarizing everything that has been said regarding the pathogenesis of various types of shock, it is legitimate to draw the following conclusions:

The most general mechanisms and patterns of development of all forms of shock are the same. They are based on the reflex principle of the body’s responses and the staged nature of the development of all forms of the process.

With different shock processes, the nature of the stimuli is different, the place of their application is the nature of the receptors exposed to irritation, perhaps the initial processes on the periphery, which serve as the cause and source of primary irritation, are different, but the leading role in the development of shock in all cases belongs to disorders in the central nervous system.

The mechanism of shock development consists of 3 components:

disorders of 1) regulation, 2) metabolism and 3) their circulatory support.

The main pathogenetic link at all stages of shock is the inconsistency of changes in metabolism and its circulatory support, which arises as a result of disorders of nervous and humoral regulation.

The classic description of shock made by I.I. Pirogov, was included in almost all shock manuals. For a long time, research on shock was carried out by surgeons. The first experimental work in this area was carried out only in 1867. Until now, there is no unambiguous definition of the concept of “shock” for pathophysiologists and clinicians. From the point of view of pathophysiology, the most accurate is the following: traumatic shock is a typical pathological process that occurs as a result of damage to organs, irritation of receptors and nerves of injured tissue, blood loss and the entry of biologically active substances into the blood, that is, factors that together cause excessive and inadequate reactions of adaptive systems, especially the sympathetic-adrenal system, persistent violations of the neuroendocrine regulation of homeostasis, especially hemodynamics, violations of specific functions of damaged organs, disorders of microcirculation, oxygen regime of the body and metabolism. It should be noted that the general etiology of traumatic shock in the form of a stable theory has not yet been developed. Nevertheless, there is no doubt that all the main factors of etiology take part in the development of shock: the traumatic factor, the conditions in which the injury was received, the body’s response. Environmental conditions are of great importance for the development of traumatic shock. Traumatic shock is promoted by: overheating, hypothermia, malnutrition, mental trauma (it has long been noted that in the defeated, shock develops faster and is more severe than in the winners).

The significance of the state of the body for the occurrence of shock (data are still scarce): 1. Heredity - these data are difficult to obtain in humans, but they are available in experimental animals. Thus, dogs’ resistance to injury depends on the breed. At the same time, dogs of pure lines are less resistant to injury than mongrels. 2. Type of nervous activity - animals with increased excitability are less resistant to injury and shock develops after a minor injury. 3. Age – shock is easier to get in young animals (puppies) and more difficult to treat than in adults. In old and senile age, trauma affects a significantly weakened body, characterized by the development of vascular sclerosis, hyporeactivity of the nervous system, endocrine system, so shock develops more easily and mortality is higher. 4. Diseases preceding the injury. The development of shock is promoted by: hypertension; neuropsychic stress; physical inactivity; blood loss preceding the injury. 5. Alcohol intoxication - on the one hand, increases the likelihood of injury (nervous dysfunction), and at the same time is used as an anti-shock liquid. But even here it should be remembered that with chronic alcoholism, changes are observed in the nervous and endocrine systems, leading to a decrease in resistance to injury. Discussing the role of various pathogenetic moments in the origin of traumatic shock, most researchers note the different times of their inclusion in the general mechanism of development of the process and their unequal significance in different periods of shock. Thus, it is quite obvious that consideration of traumatic shock is unthinkable without taking into account its dynamics - its phase development.

There are two phases in the development of traumatic shock: erectile, occurring after the injury and manifested by activation of functions, and torpid, expressed by inhibition of functions (both phases were described by N.I. Pirogov, and substantiated by N.N. Burdenko). The erectile phase of shock (from the Latin erigo, erectum - straighten, raise) is a phase of generalized excitation. In recent years it has been called adaptive, compensatory, non-progressive, early. During this phase, activation of specific and nonspecific adaptive reactions is observed. It is manifested by pallor of the integument and mucous membranes, increased arterial and venous pressure, tachycardia; sometimes urination and defecation. These reactions have an adaptive orientation. They provide, under extreme conditions, the delivery of oxygen and metabolic substrates to tissues and organs, and the maintenance of perfusion pressure. As the degree of damage increases, these reactions become excessive, inadequate and uncoordinated, which significantly reduces their effectiveness. This largely determines the severe or even irreversible self-aggravating course of shock conditions. Consciousness is not lost during shock. Usually there is nervous, mental and motor arousal, manifested by excessive fussiness, agitated speech, increased responses to various stimuli (hyperreflexia), and screaming. In this phase, as a result of generalized excitation and stimulation of the endocrine apparatus, metabolic processes are activated, while their circulatory support is insufficient. In this phase, prerequisites arise for the development of inhibition in the nervous system, circulation disorders, and oxygen deficiency occurs. The erectile phase is short-lived and usually lasts minutes. If the adaptation processes are insufficient, the second stage of shock develops.

The torpid phase of shock (from the Latin torpidus - sluggish) is a phase of general inhibition, manifested by physical inactivity, hyporeflexia, significant circulatory disorders, in particular arterial hypotension, tachycardia, respiratory disorders (tachypnea at the beginning, bradypnea or periodic breathing at the end), oliguria, hypothermia etc. In the torpid phase of shock, metabolic disorders are aggravated due to disorders of neurohumoral regulation and circulatory support. These disorders are not the same in different organs. The torpid phase is the most typical and prolonged phase of shock; its duration can range from several minutes to many hours. Currently, the torpid phase is called the stage of disadaptation (decompensation). At this stage, two substages are distinguished: progressive (consisting in the depletion of compensatory reactions and tissue hypoperfusion) and irreversible (during which changes incompatible with life develop).

In addition to the erectile and torpid phases of traumatic shock in severe shock ending in death, it is advisable to distinguish the terminal phase of shock, thereby emphasizing its specificity and difference from the pre-mortem stages of other pathological processes, usually united by the general term “terminal conditions”. The terminal phase is characterized by certain dynamics: it begins to be revealed by disorders of external respiration (Biot or Kussmaul breathing), instability and a sharp decrease in blood pressure, and slowing of the pulse. The terminal phase of shock is characterized by a relatively slow development, and therefore a greater depletion of adaptation mechanisms, more significant than, for example, with blood loss, intoxication, and more profound dysfunction of organs. The restoration of these functions during therapy occurs more slowly.

Traumatic shock should be classified according to the time of development and severity. Based on the time of development, primary shock and secondary shock are distinguished. Primary shock develops as a complication soon after the injury and may subside or lead to the death of the victim. Secondary shock usually occurs several hours after the patient recovers from primary shock. The cause of its development is most often additional trauma due to poor immobilization, difficult transportation, premature surgery, etc. Secondary shock is significantly more severe than primary shock, since it develops against the background of very low adaptive mechanisms of the body, which were exhausted in the fight against primary shock, therefore mortality in secondary shock is significantly higher. According to the severity of the clinical course, mild shock, moderate shock and severe shock are distinguished. Along with this, shock is divided into four degrees. This division is based on the level of systolic blood pressure. I degree of shock is observed when the maximum blood pressure is above 90 mm Hg. Art. – mild stupor, tachycardia up to 100 beats/min, urination is not impaired. Blood loss: 15–25% of the total blood volume. II degree – 90–70 mm Hg. Art., stupor, tachycardia up to 120 beats/min, oliguria. Blood loss: 25–30% of the total blood volume. III degree – 70–50 mm Hg. Art., stupor, tachycardia more than 130–140 beats/min, no urination. Blood loss: more than 30% of the total blood volume. IV degree – below 50 mmHg. Art., coma, pulse in the periphery is not detected, the appearance of pathological breathing, multiple organ failure, areflexia. Blood loss: more than 30% of the total blood volume. Should be regarded as a terminal condition. The clinical picture of shock is influenced by the type of nervous system, gender, age of the victim, concomitant pathology, infectious diseases, and a history of trauma accompanied by shock. An important role is played by blood loss, dehydrating diseases and conditions that affect the blood volume and lay the basis for hemodynamic disorders. A shock index can be obtained to obtain a certain idea of the degree of decrease in blood volume and the depth of hypovolemic disorders. It can be calculated using the following formula: shock index = pulse rate / systolic blood pressure. Normally, the shock index is 0.5. In the case of an increase in the index to 1 (pulse and blood pressure are equal to 100), the approximately decrease in blood volume is equal to 30% of the expected value; when it increases to 1.5 (pulse is 120, blood pressure is 80) the blood volume is 50% of the expected value, and with shock index values 2.0 (pulse – 140, blood pressure – 70), the volume of circulating blood in active circulation is only 30% of what it should be, which, of course, cannot provide adequate perfusion of the body and leads to a high risk of death for the victim. The main pathogenetic factors of traumatic shock can be identified as follows: inadequate impulses from damaged tissues; local blood and plasma loss; the entry into the blood of biologically active substances resulting from cell destruction and oxygen starvation of tissues; loss or dysfunction of damaged organs. Moreover, the first three factors are nonspecific, that is, inherent in any injury, and the last characterizes the specificity of the injury and the shock that develops.

In its most general form, the pathogenesis of shock is presented as follows. The traumatic factor acts on organs and tissues, causing their damage. As a result, cell destruction occurs and their contents escape into the intercellular environment; other cells are subject to contusion, as a result of which their metabolism and inherent functions are disrupted. Primary (due to the action of a traumatic factor) and secondary (due to changes in the tissue environment) numerous receptors in the wound are irritated, which is subjectively perceived as pain, but objectively characterized by numerous reactions of organs and systems. Inadequate impulses from damaged tissues have a number of consequences. 1. As a result of inadequate impulses from damaged tissues, a pain dominant is formed in the nervous system, which suppresses other functions of the nervous system. Along with this, a typical defensive reaction occurs with stereotypical autonomic accompaniment, since pain is a signal to flee or fight. The most important components of this autonomic reaction are: the release of catecholamines, increased blood pressure and tachycardia, increased breathing, activation of the hypothalamic-pituitary-adrenal system. 2. The effects of painful stimulation depend on its intensity. Weak and moderate irritation causes stimulation of many adaptive mechanisms (leukocytosis, phagocytosis, increased function of the SFM, etc.); strong irritations inhibit adaptive mechanisms. 3. Reflex tissue ischemia plays an important role in the development of shock. In this case, under-oxidized products accumulate, and the pH decreases to values borderline acceptable for life. On this basis, microcirculation disorders, pathological blood deposition, and arterial hypotension occur. 4. Pain and the entire situation at the time of injury certainly cause emotional stress, mental tension, and a feeling of anxiety about danger, which further enhances the neurovegetative reaction.

The role of the nervous system. When the body is exposed to a damaging mechanical agent in the damaged area, various nerve elements are irritated, not only receptors, but also other elements - nerve fibers passing through the tissues that are part of the nerve trunks. While the receptors have a certain specificity in relation to the stimulus, characterized by differences in the threshold value for different stimuli, the nerve fibers in relation to mechanical stimulation do not differ so sharply from each other, therefore mechanical stimulation causes excitation in conductors of various types of sensitivity, and not only painful or tactile. This is precisely why injuries accompanied by crushing or rupture of large nerve trunks are characterized by more severe traumatic shock. The erectile phase of shock is characterized by generalization of excitation, which is externally manifested in motor restlessness, speech excitation, screaming, and increased sensitivity to various stimuli. Excitation also covers the autonomic nerve centers, which is manifested by an increase in the functional activity of the endocrine apparatus and the release of catecholamines, adaptive and other hormones into the blood, stimulation of heart activity and an increase in the tone of resistance vessels, activation of metabolic processes. Prolonged and intense impulses from the site of injury, and then from organs with impaired functions, changes in the lability of nerve elements due to disorders of blood circulation and oxygen regime determine the subsequent development of the inhibitory process. The irradiation of excitation—its generalization—is a necessary prerequisite for the occurrence of inhibition. Of particular importance is the fact that inhibition in the zone of the reticular formation protects the cerebral cortex from the flow of impulses from the periphery, which ensures the safety of its functions. At the same time, elements of the reticular formation that facilitate the conduction of impulses (RF+) are more sensitive to circulatory disorders than those that inhibit the conduction of impulses (RF–). It follows from this that circulatory disorders in this area should contribute to a functional blockade of impulse conduction. Gradual inhibition extends to other levels of the nervous system. It tends to deepen due to impulses from the area of injury.

The role of the endocrine system.
Traumatic shock is also accompanied by changes in the endocrine system (in particular, the hypothalamic-pituitary-adrenal system). During the erectile phase of shock, the content of corticosteroids in the blood increases, and during the torpid phase, their amount is reduced. However, the adrenal cortex remains responsive to externally administered ACTH. Consequently, the inhibition of the cortical layer is largely due to the insufficiency of the pituitary gland. Hyperadrenalineemia is very typical for traumatic shock. Hyperadrenalineemia, on the one hand, is a consequence of intense afferent impulses caused by damage, on the other, a reaction to the gradual development of arterial hypotension.

Local blood and plasma loss.
With any mechanical injury, there is a loss of blood and plasma, the extent of which is very variable and depends on the degree of tissue trauma, as well as on the nature of vascular damage. Even with a minor injury, exudation into the injured tissue is observed due to the development of an inflammatory reaction, and hence loss of fluid. However, the specificity of traumatic shock is still determined by neuropainful injury. Neuropainful injury and blood loss are synergistic in their effect on the cardiovascular system. With painful stimulation and loss of blood, vasospasm and the release of catecholamines first occur. With blood loss immediately, and with painful stimulation later, the volume of circulating blood decreases: in the first case due to exit from the vascular bed, and in the second - as a result of pathological deposition. It should be noted that even small bloodletting (1% of body weight) sensitizes (increases the body’s sensitivity) to mechanical damage.

Circulatory disorders.
The very concept of “shock” includes obligatory and severe hemodynamic disturbances. Hemodynamic disturbances during shock are characterized by sharp deviations in many parameters of the systemic circulation. Disorders of systemic hemodynamics are characterized by three cardinal signs - hypovolemia, decreased cardiac output and arterial hypotension. Hypovolemia has always been considered important in the pathogenesis of traumatic shock. On the one hand, it is caused by blood loss, and on the other, by the retention of blood in capacitive vessels (venules, small veins), capillaries - by its deposition. The exclusion of some blood from circulation can be clearly detected already at the end of the erectile shock phase. By the beginning of the development of the torpid phase, hypovolemia is even more pronounced than in subsequent periods. One of the most typical symptoms of traumatic shock is phase changes in blood pressure - its increase in the erectile phase of traumatic shock (the tone of resistive and capacitive vessels increases, as evidenced by arterial and venous hypertension), as well as a short-term increase in the volume of circulating blood, combined with a decrease in the capacity of the functioning vascular bed of organs. The increase in blood pressure, typical for the erectile phase of traumatic shock, is the result of an increase in total peripheral vascular resistance due to activation of the sympathoadrenal system. An increase in the tone of resistive vessels is combined with the activation of arteriovenous anastomoses and the rejection of blood from the system of high pressure vessels (arterial bed) into the system of low pressure vessels (venous bed), which leads to an increase in venous pressure and prevents the outflow of blood from the capillaries. If we take into account the fact that most capillaries do not have sphincters at their venous end, then it is not difficult to imagine that under such conditions not only direct, but also retrograde filling of the capillaries is possible. Numerous researchers have shown that hypovolemia limits afferent impulses from baroreceptors (stretch receptors) of the aortic arch and sinocarotid zone, as a result of which the pressor formations of the vasomotor center are excited (disinhibited) and spasm of arterioles occurs in many organs and tissues. Sympathetic efferent impulses to the blood vessels and heart are enhanced. As blood pressure decreases, tissue blood flow decreases, hypoxia increases, which causes impulses from tissue chemoreceptors and further activates the sympathetic effect on the vessels. The heart empties more completely (residual volume decreases), and tachycardia also occurs. A reflex also arises from the vascular baroreceptors, leading to an increased release of adrenaline and norepinephrine by the adrenal medulla, the concentration of which in the blood increases 10-15 times. In a later period, when renal hypoxia develops, vascular spasm is maintained not only by increased secretion of catecholamines and vasopressin, but also by the release of renin by the kidneys, which is the initiator of the renin-angiotensin system. It is believed that this generalized vasoconstriction does not involve the vessels of the brain, heart and liver. Therefore, this reaction is called centralization of blood circulation. Peripheral organs are increasingly suffering from hypoxia, as a result of which metabolism is disrupted and under-oxidized products and biologically active metabolites appear in the tissues. Their entry into the blood leads to acidosis of the blood, as well as the appearance in it of factors that specifically inhibit the contractility of the heart muscle. Another mechanism is also possible here. The development of tachycardia leads to a reduction in diastole time - the period during which coronary blood flow occurs. All this leads to disruption of myocardial metabolism. With the development of the irreversible stage of shock, the heart can also be affected by endotoxins, lysosomal enzymes and other biologically active substances specific to this period. Thus, blood and plasma loss, pathological blood deposition, and fluid extravasation lead to a decrease in the volume of circulating blood and a decrease in venous blood return. This, in turn, along with metabolic disorders in the myocardium and a decrease in the performance of the heart muscle leads to hypotension, characteristic of the torpid phase of traumatic shock. Vasoactive metabolites that accumulate during tissue hypoxia disrupt the function of vascular smooth muscles, which leads to a decrease in vascular tone, and therefore to a drop in the overall resistance of the vascular bed and, again, to hypotension.
Disorders of capillary blood flow deepen as a result of a violation of the rheological properties of blood, aggregation of red blood cells, which occurs as a result of increased activity of the coagulation system and thickening of the blood due to the release of fluid into the tissue. Breathing disorders. In the erectile stage of traumatic shock, frequent and deep breathing is observed. The main stimulating factor is irritation of the receptors of injured tissues, which causes stimulation of the cerebral cortex and subcortical centers, and the respiratory center of the medulla oblongata is also excited.
In the torpid phase of shock, breathing becomes more rare and superficial, which is associated with depression of the respiratory center. In some cases, as a result of progressive brain hypoxia, periodic respiration of the Cheyne-Stokes or Biot type appears. In addition to hypoxia, various humoral factors have an inhibitory effect on the respiratory center - hypocapnia (caused by hyperventilation - but later CO2 accumulates), low pH. The development of hypoxia, one of the very important aspects of the pathogenesis of traumatic shock, is closely related to circulatory and respiratory disorders. In the genesis of shock hypoxia, the hemic component also occupies a certain place, caused by a decrease in the oxygen capacity of the blood due to its dilution and aggregation of red blood cells, as well as external respiration disorders, but the main importance still belongs to tissue perfusion and the redistribution of blood flow between terminal vessels.

Abnormalities in the lungs and the effects they cause are combined into a symptom complex called respiratory distress syndrome. This is an acute disorder of pulmonary gas exchange with life-threatening severe hypoxemia as a result of a decrease to a critical level and below the number of normal respirons (respiron is the terminal or final respiratory unit), which is caused by negative neurohumoral influences (neurogenic spasm of pulmonary microvessels with pathological pain), damage to the pulmonary capillary endothelium with cytolysis and destruction of intercellular connections, migration of blood cells (primarily leukocytes), plasma proteins into the pulmonary membrane, and then into the lumen of the alveoli, the development of hypercoagulation and thrombosis of the pulmonary vessels.

Metabolic disorders. Energy exchange.
Shock of various etiologies through microcirculation disorders and destruction of the histohematic barrier (exchange capillary - interstitium - cell cytosol) critically reduces oxygen delivery to mitochondria. As a result, rapidly progressing disorders of aerobic metabolism occur. The links in the pathogenesis of dysfunctions at the level of mitochondria in shock are: - swelling of mitochondria; - disorders of mitochondrial enzyme systems due to a deficiency of necessary cofactors; - decrease in magnesium content in mitochondria; - increase in calcium content in mitochondria; - pathological changes in the content of sodium and potassium in mitochondria; - disorders of mitochondrial functions due to the action of endogenous toxins (free fatty acids, etc.); - free radical oxidation of mitochondrial membrane phospholipids. Thus, during shock, the accumulation of energy in the form of high-energy phosphorus compounds is limited. A large amount of inorganic phosphorus accumulates, which enters the plasma. Lack of energy disrupts the function of the sodium-potassium pump, causing excess sodium and water to enter the cell and potassium to leave the cell. Sodium and water cause mitochondria to swell, further uncoupling respiration and phosphorylation. As a result of decreased energy production in the Krebs cycle, the activation of amino acids is limited, and as a result, protein synthesis is inhibited. A decrease in ATP concentration slows down the combination of amino acids with ribonucleic acids (RNA), the function of ribosomes is disrupted, resulting in the production of abnormal, incomplete peptides, some of which may be biologically active. Severe acidosis in the cell causes rupture of lysosome membranes, as a result of which hydrolytic enzymes enter the protoplasm, causing the digestion of proteins, carbohydrates, and fats. The cell dies. As a result of insufficient cell energy and metabolic disorders, amino acids, fatty acids, phosphates, and lactic acid enter the blood plasma. Apparently, mitochondrial dysfunctions (like any pathological processes) develop in different organs and tissues asynchronously, mosaically. Damage to mitochondria and disorders of their functions are especially pronounced in hepatocytes, while in neurons of the brain they remain minimal even in decompensated shock.
It should be noted that mitochondrial damage and dysfunction are reversible in compensated and decompensated shock and are reversed by rational analgesia, infusions, oxygen therapy and hemorrhage control. Carbohydrate metabolism. During the erectile phase of traumatic shock, the concentration of insulin antagonists, catecholamines, which stimulate the breakdown of glycogen, glucocorticoids, which enhance the processes of gluconeogenesis, thyroxine and glucagon, increases in the blood as a result of increased activity of the endocrine glands. In addition, the excitability of the sympathetic nervous system (hypothalamic centers) is increased, which also contributes to the development of hyperglycemia. In many tissues, glucose consumption is inhibited. In general, a false-diabetic picture is revealed. In the later stages of shock, hypoglycemia develops. Its origin is associated with the complete use of liver glycogen reserves available for consumption, as well as a decrease in the intensity of gluconeogenesis due to the use of substrates necessary for this and relative (peripheral) corticosteroid deficiency.
Lipid metabolism. Changes in carbohydrate metabolism are closely associated with lipid metabolism disorders, which manifest themselves in the torpid phase of shock as ketonemia and ketonuria. This is explained by the fact that fats (as one of the main energy sources) are mobilized from the depot during shock (their concentration in the blood increases), and oxidation is not complete.
Protein metabolism. A manifestation of its disturbance is an increase in the content of non-protein nitrogen in the blood, mainly due to polypeptide nitrogen and, to a lesser extent, urea nitrogen, the synthesis of which is disrupted with the development of shock. Changes in the composition of serum proteins during traumatic shock are expressed by a decrease in their total amount, mainly due to albumin. The latter may be associated both with metabolic disturbances and with changes in vascular permeability. It should be noted that with the development of shock, the content of α-globulins in the serum increases, which, as is known, is directly related to the vasoactive properties of the blood. The accumulation of nitrogenous products and changes in the ionic composition of plasma contribute to impaired renal function. Oliguria, and in severe cases of shock, anuria are constant during this process. Renal dysfunction usually corresponds to the severity of shock. It is known that with a decrease in blood pressure to 70-50 mm Hg. Art. the kidneys completely stop filtering in the glomerular apparatus of the kidney due to changes in the relationships between hydrostatic, colloidosmotic and capsular pressure. However, in traumatic shock, renal dysfunction is not solely a consequence of arterial hypotension: shock is characterized by limitation of cortical circulation due to increased vascular resistance and shunting through the juxtaglomerular pathways. This is determined not only by a decrease in cardiac performance, but also by an increase in the tone of the vessels of the cortical layer.
Ion exchange. Significant shifts are detected in the ionic composition of the plasma. With traumatic shock, a gradual convergence occurs, the concentration of ions in the cells and extracellular fluid, while normally the ions K+, Mg2+, Ca2+, HPO42-, PO43- predominate in the cells, and in the extracellular fluid Na+, C1-, HCO3-. Receipt of biologically active substances into the blood. For the subsequent course of the process, the release of active amines from cells, which are chemical mediators of inflammation, is of great importance. Currently, over 25 such mediators have been described. The most important of them, appearing immediately after damage, are histamine and serotonin. With extensive tissue damage, histamine can enter the general bloodstream, and since histamine causes dilation of precapillaries and spasm of veins without directly affecting the capillary bed, this leads to a decrease in peripheral vascular resistance and a drop in blood pressure. Under the influence of histamine, channels and gaps are formed in the endothelium, through which blood components, including cellular elements (leukocytes and erythrocytes), penetrate into the tissues. As a result of this, exudation and intercellular edema occur. Under the influence of injury, the permeability of vascular and tissue membranes increases, but still, due to circulatory disorders, the absorption of various substances from injured tissues slows down. Enzymes of lysosomes of tissue cells and neutrophils play a major role in the development of secondary alteration. These enzymes (hydrolases) have pronounced proteolytic activity. Along with these factors, plasma kinins (bradykinin), as well as prostaglandins, play a certain role in circulatory disorders. These factors also affect the microcirculation system, causing expansion of arterioles, capillaries and an increase in their permeability, which occurs first (mainly in venules) due to the formation of intercellular gaps and transendothelial channels. Later, the permeability of the capillary and precapillary sections of the vascular bed changes.

A few words about wound toxemia. The issue of wound toxin has not been finally resolved. However, it is firmly established that toxic substances cannot enter the blood from injured tissues, because reabsorption in them is reduced. The source of toxic substances is the extensive zone of tissue contusion around the wound channel. It is in this zone that under the influence of potassium, histamine, serotonin, lysosomal enzymes, ATP, AMP, vascular permeability sharply increases. The toxin is formed within 15 minutes after ischemia, but has a relative molecular weight of 12,000 and is a product of intense protein breakdown. Administration of this toxin to intact animals leads to hemodynamic disorders typical of shock. The vicious circles that form during traumatic shock can be represented in the form of a diagram shown in Figure 1. Fig. 1. The main vicious circles in shock. Dysfunctions of damaged organs. Most researchers consider shock to be a functional pathology, although an organic component always plays a role in etiology and pathogenesis, which includes a decrease in the volume of circulating blood and, consequently, a decrease in the number of red blood cells.
A significant factor complicating the analysis of the pathogenesis of shock in the clinic is the presence of organic damage, which can accelerate the development of shock and modify its course. Thus, damage to the lower extremities, limiting the mobility of the wounded, forces them to take a horizontal position, often on the cold ground, which, causing general cooling, provokes the development of shock. When the maxillofacial area is injured, victims lose a large amount of saliva, and along with it water and protein, which, when it is difficult to take liquids and food, contributes to the development of hypovolemia and blood thickening. With traumatic brain injuries, symptoms of brain dysfunction occur, consciousness is lost, and excessive vasospasm occurs, which often masks hypovolemia. When the pituitary gland is damaged, neuroendocrine regulation is sharply disrupted, which in itself causes the development of shock and complicates the course of the post-shock period. Fundamentals of pathogenetic therapy of shock The complexity of the pathogenesis of traumatic shock, the variety of disturbances in the functioning of many body systems, and differences in ideas about the pathogenesis of shock determine a significant difference in recommendations for the treatment of this process. We will focus on established things. Experimental studies allow us to determine possible directions in the prevention of traumatic shock. For example, the use of certain drug complexes before severe mechanical injury prevents the development of shock. Such complexes include the combined use of drugs (barbiturates), hormones, and vitamins. Long-term stimulation of the pituitary gland-adrenal cortex system with the introduction of ACTH increases the resistance of animals to shockogenic injury; the introduction of ganglion blockers also has a preventive effect. However, situations in which shock prevention is appropriate may not occur very often. Much more often we have to deal with the treatment of developed traumatic shock and, unfortunately, not always in its early periods, but in most cases in its later stages. The basic principle of treating shock is the complexity of therapy. Taking into account the phases of shock development is important in the treatment of shock. The treatment carried out should be as fast and vigorous as possible. This requirement also determines the methods of administration of certain medications, most of which are administered directly into the vascular bed. When treating shock in the erectile phase, when circulatory disorders have not yet fully developed, deep hypoxia and advanced metabolic disorders have not yet occurred, measures should be limited to preventing their development. During this phase, means that limit afferent impulses are widely used; various types of novocaine blockades, analgesics, neuroplegics, narcotic substances. Analgesics that inhibit impulse transmission, suppress autonomic reactions, and limit the feeling of pain are indicated in early periods of shock. An important point limiting impulses from the site of damage is rest of the damaged area (immobilization, bandages, etc.). In the erectile phase of shock, it is recommended to use saline solutions containing neurotropic and energetic substances (Popov, Petrov, Filatov liquids, etc.). Significant disorders of circulation, tissue respiration and metabolism that occur in the torpid phase of shock require various measures aimed at their correction. To correct circulatory disorders, blood transfusions or blood substitutes are used. In severe shock, intra-arterial transfusions are more effective. Their high effectiveness is associated with stimulation of vascular receptors, increased capillary blood flow and the release of part of the deposited blood. Due to the fact that during shock there is predominantly deposition of formed elements and their aggregation, it seems very promising to use low molecular weight colloidal plasma substitutes (dextrans, polyvinol), which have a disaggregating effect and reduce blood viscosity at low shear stresses. Caution should be exercised when using vasopressor agents. Thus, the introduction of one of the most common vasopressor substances, norepinephrine, in the initial period of the torpid phase slightly increases the minute volume of blood circulation due to the release of part of the deposited blood and improves blood supply to the brain and myocardium. The use of norepinephrine in later periods of shock even aggravates the centralization of blood circulation characteristic of it. Under these conditions, the use of norepinephrine is advisable only as an “emergency” remedy. The use of saline plasma-substituting solutions, although it leads to a temporary revival of blood flow, still does not provide a long-term effect. These solutions, with significant disturbances in capillary blood flow and changes in the ratios of colloid-osmotic and hydrostatic pressures characteristic of shock, leave the vascular bed relatively quickly. Hormones - ACTH and cortisone, administered to normalize metabolic processes, have a noticeable effect on blood flow during traumatic shock. During the development of shock, relative and then absolute adrenal insufficiency is detected first. In light of these data, the use of ACTH appears to be more appropriate in the early stages of shock or in its prevention. Glucocorticoids administered in the torpid phase have a diverse effect. They change the response of blood vessels to vasoactive substances, in particular they potentiate the effect of vasopressors. In addition, they reduce vascular permeability. And yet, their main effect is associated with the influence on metabolic processes and, above all, on the metabolism of carbohydrates. Restoration of oxygen balance in conditions of shock is ensured not only by restoration of circulation, but also by the use of oxygen therapy. Recently, oxygen barotherapy has also been recommended. In order to improve metabolic processes, vitamins are used (ascorbic acid, thiamine, riboflavin, pyridoxine, calcium pangamate). Due to the increased resorption of biogenic amines and, above all, histamine from damaged tissues, the use of antihistamines may be important in the treatment of traumatic shock. An essential place in the treatment of shock is occupied by the correction of acid-base balance. Acidosis is typical of traumatic shock. Its development is determined by both metabolic disorders and the accumulation of carbon dioxide. The development of acidosis is also facilitated by disruption of excretory processes. To reduce acidosis, the use of sodium bicarbonate is recommended; some consider the use of sodium lactate or Tris buffer to be better.